a study of intradialytic complications in patients...
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A STUDY OF INTRADIALYTIC COMPLICATIONS IN PATIENTS
UNDERGOING HEMODIALYSIS
A DISSERTATION SUBMITTED TOTHE TAMIL NADU DR. M.G.R MEDICAL UNIVERSITY
CHENNAI, TAMIL NADU
BYDr. PRIYADHARSHINI.S.,
IN PARTIAL FULFILMENT OF THE REQUIREMENTSFOR THE AWARD OF THE DEGREE OFDOCTOR OF MEDICINE - BRANCH I
(GENERAL MEDICINE)
TIRUNELVELI MEDICAL COLLEGE HOSPITALTIRUNELVELI – 11, TAMIL NADU
MAY 2019
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BONAFIDE CERTIFICATE
This is to certify that this dissertation entitled “A STUDY OF
INTRADIALYTIC COMPLICATIONS IN PATIENTS UNDERGOING
HEMODIALYSIS” submitted by Dr. PRIYADHARSHINI.S., to The Tamilnadu
Dr. M.G.R Medical University, Chennai, in partial fulfilment for the award of M.D
Degree (GENERAL MEDICINE) is a bonafide work carried out by her under my
guidance and supervision during the course of studyfrom 2015 to 2019.
Prof. Dr. L. RAJAGOPALA MARTHANDAM, M. D
Unit ChiefDepartment of MedicineTirunelveli Medical CollegeTirunelveli – 627011
Prof. Dr. M. RAVICHANDRAN, M. D
Professor & HODDepartment of MedicineTirunelveli Medical CollegeTirunelveli – 627011
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CERTIFICATE
This is to certify that this dissertation entitled “A STUDY OF
INTRADIALYTIC COMPLICATIONS IN PATIENTS UNDERGOING
HEMODIALYSIS” submitted by Dr. PRIYADHARSHINI.S., to The Tamilnadu
Dr. M.G.R Medical University, Chennai, in partial fulfilment for the award of M.D
Degree (GENERAL MEDICINE) is a bonafide work carried out by her during the
course of studyfrom 2015 to 2019. This dissertation, partially or fully hasn’t been
submitted for any other degree or diploma of this university or other.
DATE:PLACE: TIRUNELVELI
Dr. S. M. KANNAN, M. S, MchThe Dean
Tirunelveli Medical CollegeTirunelveli – 627011
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DECLARATION
I solemnly declare that the dissertation titled “A STUDY OF
INTRADIALYTIC COMPLICATIONS IN PATIENTS UNDERGOING
HEMODIALYSIS”is prepared by me under guidance of Prof.Dr. L. RAJAGOPALA
MARTHANDAM, M.D. The dissertation is submitted to The TamilnaduDr. M.G.R
Medical University towards partial fulfilment of requirements for the award of M.D
Degree (Branch I) in General Medicine. I also declare that this bonafide work or a part
of this work was not submitted by me or others for any award, degree, diploma to any
university, found either in India or abroad.
Place: Tirunelveli
Date :
Dr. PRIYADHARSHINI.S
Postgraduate student
M.D General Medicine
Department of Medicine
Tirunelveli Medical College
Tirunelveli - 627011
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ACKNOWLEDGEMENT
First of all I express my sincere gratitude and indebtedness to our beloved
Prof.Dr.L. RajagopalaMarthandam M.D., Unit Chief, 3rd Medical unit, Tirunelveli
Medical College, whose constant encouragement and guidance shaped this study. His
learned guidance, reasoning beyond comparison, and the virtue of punctuality, which
he instils in everyone around him, have helped me, more than words can say, in the
successful completion of my study.
My sincere thanks and gratitude to my professors and teachers
Dr.J.Bharath M.D, Dr.P.Renuga M.D, Dr.Meenakumari M.D, Dr.Veerapandiyan
M.D for their valuable support and encouragement throughout the period of my study.I
would also like to express my sincere thanks toDr.Ramasubramanian MD
DM(Nephro) and Dr.P.K.Senthilkumar MD DM(Nephro) for their invaluable
guidance and affection.
A special word of thanks to my seniors Dr. Danny, Dr.Lakshmi,
Dr.Vinoj for their valuable advice and inputs which helped in shaping this work.My
colleagues Dr.SusanGeorge,Dr.Nandhini, Dr.Bhavani,Dr.Gopinath,Dr.Parthiban,
Dr.Jayaprakash, Dr. Irfan, Dr.Arunagiri, Dr. Akbar Sha, who co-operated
immensely in the conduct of this study, deserve special mention.
Dr.Kathirvel, Dr.Padmapriya, Dr. Srinivasan, Dr. Jai Praveen,
Dr.Shanavaz, Dr.Murugan, my juniors, were of great support throughout my study
and I cannot thank them enough for their help in managing the ward and clinical work
when I was going through my tough times with the study.
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I am indebted to the ward sisters and other supporting staff for their help in managing
the ward and their constant support throughout my course.
I would also like to express my heartfelt gratitude to Dr.Amudhan Arvind for
helping me with the statistical analysis of my study.
I sincerely thank the Dean and the Medical Superintendent of this institute
for allowing me to carry out this study.
I would like to thank all the friends who wished, prayed, supported and
helped me in all ways possible during the difficult times of the study.
A thanksgiving note will be nowhere near complete without a mention of
my deepest gratitude and love for my parents, my brothers and my husband, Dr.
M.MuthuPrakash, for their constant encouragement in all my endeavours even through the
trying times.
Above all, I thank all the patients who were willing participants in the
study, in spite of their sufferings and I sincerely pray for their welfare.
Last but not the least I thank almighty GOD for giving me wisdom,
favours and blessings.
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CERTIFICATE – II
This is to certify that I have verified this dissertation work titled “A STUDY OF
INTRADIALYTIC COMPLICATIONS IN PATIENTS UNDERGOING
HEMODIALYSIS” of the candidate Dr.PRIYADHARSHINI.S.,with registration
Number 201511356 for the award of M.D. in the branch of General Medicine. I
personally verified the urkund.com website for the purpose of plagiarism check. I found
that theuploaded thesis file contains from introduction to conclusion page and
resultshows 7 percentageof plagiarism in the dissertation.
Guide & Supervisor sign with Seal.
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SI.NO CONTENTS PAGE NO
1 INTRODUCTION 1
2 AIMS AND OBJECTIVES 2
3 REVIEW OF LITERATURE 3
4 MATERIALS AND METHODS 38
5 OBSERVATIONS AND RESULTS 41
6 DISCUSSION 74
7 SUMMARY 76
8 CONCLUSION 77
9 BIBLIOGRAPHY
10 ANNEXURES
Proforma
Consent Form
Master Chart
Abbreviations
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ABBREVIATIONS
HD - Haemodialysis
AKJ - Acute Kidney Injury
CKD - Chronic Kidney Disease
AV Fistula - Arterio Venous Fistula
BUN - Blood Urea Nitrogen
CNS - Central Nervous System
CSF - Cerebro spinal Fluid
PTH - Parathyroid Hormone
FFP - Fresh Frozen plasma
ESRD - End stage renal disease
UVB - Ultraviolet B
CAD - Coronary artery Disease
BP - Blood Pressure
SHT - Systemic Hypertension
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INTRODUCTION
Hemodialysis is the process of removing solutes from the body
using a semipermeable artificial membrane when blood comes in contact
with the same during extracorporeal circulation. It maintains the fluid and
electrolytes in normal homeostasis.The first hemodialysis was
successfully done by Dr.WillamKolff.
In Hemodialysis,the dialysis machine and dialyser are used to filter
the blood and remove the toxins and excess fluid from the body. The
components of haemodialysis are the Dialyzer, the composition and
delivery of the dialysate and the blood delivery system. The principle
behind Hemodialysis is ultrafiltration and diffusion.
The Hemodialysis procedure is associated with a number of
complication. The common complication are hypotension and intradialytic
hypertension, dialyzer reactions, disequilibrium syndrome, muscle
cramping other less common complications are haemolysis haemorrhage,
hypoxia, air embolism and cardiac arrhythmias.
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AIM OF THE STUDY
1. To evaluate the various intradialytic complications of Hemodiaysis
2. To identify the Incidence of the intradialytic complication among the
patients undergoing HD
3. To study the association between Kidney disease and complications
in relation to age and sex distribution
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REVIEW OF LITERATURE:
History
Graham (1805 to 1869) invented the process of solute separation in vitro
by using semipermeable membranes and the word “dialysis” was coined by
him. He was a Scottish professor of chemistry. In 1924 Haas from
Germany first used dialysis in humans. Dr. Willem Kolff, a Dutch
physician in 1944, used extracorporeal dialysis and successfully treated in
patients with acute kidney injury. Kolff was called the “Father of
Hemodialysis”.During the initial years following the introduction of
hemodialysis, complications were common due to the technical drawbacks
associated with the dialysis machines and associated water systems.
Currently, the advances in technology, particularly those in the last 20
years, have reduced the complications. However, complications caused by
the reasons other than the dialysis machine and water systems remain a
significant cause of morbidity and mortality in patients undergoing
hemodialysis.
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HEMODIALYSIS:
Hemodialysis depends on the principles of solute diffusion across
the semipermeable membrane.
Factors determining the rate of diffusive transport across the
membrane are magnitude of the concentration gradient, the surface area of
the membrane and the mass transfer coefficient of the membrane.
Smaller molecules (such as urea 60 Da) clear easily compared with larger
molecules (creatinine 113 Da).
The two types of clearance of the molecules in HD are “diffusive”
clearance and “convective” clearance.
The clearance of solutes are the judging factor for the performance of the
dialysis.
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COMPONENTS OF HEMODIALYSIS:
1. The Dialyzer
2. The composition and delivery of the Dialysate.
3. The blood delivery system.
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THE DIALYZER:
It is a plastic chamber. Hollow fibre dialyzer is commonly used and
it composed of bundles of capillary tubes and blood circulates on the
outside of the fibre bundle.
THE DIALYSATE:
The potassium concentrate varies from 0.4mmol/l and the usual
calcium concentration is 2.5meq/lit. Higher calcium concentrations are
used in hypocalcemia patients with secondary hyperparathyroidism. The
sodium concentration is 136-140 mmol/l
BLOOD DELIVERY SYSTEM:
It consists of extracorporeal circuit and the dialysis access. Blood
flow rate varies from 250 to 500ml/min. Commonly used dialysis access is
native fistula created by the anastomosis of an artery to a vein (e.g. the
bresciacimino fistula) in this cephalic vein is anastomosed end to side to
the radial artery.
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VASCULAR ACCESS:
The radio-cephalic AV fistula is the access of choice otherwise
known as Brescia-Cimino access.
Permanent catheter increases the longevity of the HD (maintanence).
Types of Vascular Access:
1. Arterio venous fistula
2. Arteriovenous grafts
Arterio-venous fistula:
Brescia and colleagues first described this procedure[1].
Pre operative – ultrasonographic images will increases the
successfulness of the AV fistula [2].
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AV fistula is created by connecting vein and artery, by two
approaches,
a. Side to side approach
b. End to side anastomosis
Arteriovenous grafts:
Advantages of this AV grafts are ease of placement and short time
requirement. adequate vein is not required in the forearm for this
procedures. Advantages of this procedure is low thrombosis rate of
graft. Primary patency rate – 12 months for around 50% individuals
[3].
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COMMON INDICATIONS FOR HEMODIALYSIS:
Chronic kidney disease (CKD) is one among the commonest health
problems faced by today’s general population. Over millions of
people throughout the world are diagnosed with CKD, and among
them many require renal replacement therapies such as dialysis and
renal transplantation. Among the predisposing factors for CKD, the
most common two causes are diabetes and hypertension, thus
increasing the prevalence rates in CKD.
The mortality rates due to CKD and its related complications would have
spiked very high in weeks duration without this protocoled approach in
“hemodialysis”.
INTRODUCTION TO INTRADIALYTIC COMPLICATIONS OF
HEMODIALYSIS:
Cardiovascular complications top among the list of complications
with the current practices in hemodialysis. Among the cardiovascular
complications, the rate of symptomatic intradialytic hypotension range
between 20% and 50%, and it remains an important problem. Another
concern is the arrhythmias associated with hemodialysis, the rate of which
is reported to be between 5% to 75%. The common and severe type of
arrhythmias include ventricular arrhythmias and ectopics. The rate of
hemodialysis-associated complex ventricular arrhythmia is around 35%.
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The second most common type of arrhythmia is atrial fibrillation, the rate
of which is 27%. Sudden cardiac death accounts for 62% of cardiac-related
deaths and it is usually attributed to arrhythmias [4].The first year of
hemodialysis is of vital importance with respect to sudden cardiac deaths,
which was evaluated in 93 of 1000 patients in the first year of hemodialysis
[5].
During the early period of introduction of dialysis therapy cramps were
observed in 24% to 86% and in contrast with current advances in dialysis
the data shows about 2% of the patients having ≥2 hemodialysis sessionsin a week suffer from cramps [6].Other common complications include
nausea, vomiting with a rate of 5% to 15%, headache with a rate of 5% to
10% and itching with a rate of 5% to 10% [7], [8]. Although cramps,
nausea, vomiting, headache and itching do not result in mortality, they
substantially deteriorate the quality of life in these patients. Although more
common during the first years following the introduction of dialysis,
disequilibrium syndrome and complications associated with dialyser, water
systems and dialysis machines are currently uncommon but may have fatal
consequences.
Hemodialysis cause many complications despite the advances in
technology. It is of great importance in early recognition and correction of
life-threatening complications. Some complications may not threaten the
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patient’s life but deteriorate the quality of life of the patients. The treatment
of these complications provides a longer life and a better quality of life for
the patients. Acute complications of hemodialysis can be classified as
follows:
o Complications associated with hemodialysis equipment
Hemodialysis device-related complications
Membrane-related complications
Water system-related complications
Vascular access-related complications
o Cardiovascular complications:
Hypotension: Fluid removal in HD depends on residual urine
output of the patient and interdialytic fluid intake with factors
like congestive heart failure, female gender and elderly people
increase the hypotension events.
Treatment: It is by temporarily reducing the rate of ultrafiltration
combined with patient being placed in Trendelenburg position.
Replacement of fluid 100 to 250ml of normal saline and (or) albumin. If
hypotension still persists, consider other causes such as pericardial
disease or myocardial injury.
Hypertension
Arrhythmias
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Pericardial effusion
Chest pain
Sudden death
o Neurological complications
Dialysis Disequilibrium syndrome: If the solution level is
rapidly reduced within a short period of time. Symptoms are
mental status changes, generalized seizures and coma.
Mild form- vomiting, headache, restlessness and easy fatigability.
Cerebrovascular accident
Consciousness changes
Headache
Seizure
Tremor
o Complications associated with use of anticoagulant therapy
Heparin associated thrombocytopenia
Bleeding diathesis
Electrolyte abnormalities
Hematologic complications
o Others
Nausea
Vomiting
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Itching
Muscle cramps: Reason for this complication is due to excessive
and rapid removal of fluid with associated hypotension and
electrolyte disturbance.
Intradialytic hypotension
Patient related factors
1. Impaired plasma volume refilling (too high ultrafiltration, autonomic
dysfunction)
2. Decreased cardiac reserve (diastolic or systolic dysfunction)
3. Impaired venous compliance
4. Autonomic dysfunction (diabetes, uremia)
5. Arrhythmias
6. Anemia
7. Drug therapy (vasodilators, ß blockers, calcium channel blockers)
8. Alteration of vasoactive substances in blood (low NO, high
endothelin-1 andangiotensin-2)
9. Eating during treatment (increased splanchnic blood flow)
10.Too low target weight estimation
Procedure associated factors:
1. Rapid decreases in plasma osmolality (relatively large surface area
membrane, highstarting BUN)
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2. Excess absolute volume and rate of fluid removal (for fluid
overload)
3. Change in serum electrolytes (hypocalcemia, hypokalemia)
4. Dialysate – acetate, warm dialysate
5. Membrane blood interaction
6. Hypoxia (partially patient related)
7. Electrolyte abnormalities
Other less common causes -
1. Pericardial tamponade
2. Myocardial infarction
3. Aortic dissection
4. Internal or external hemorrhage
5. Septicemia
6. Air embolism
7. Pneumothorax
8. Hemolysis
Pathogenesis in Intradialytic hypotension: Vascular instability during
dialysis is a multifactorial process in which procedure and patientrelated
factors may influence the decrease in plasma volume and induce an
impairment ofcardiovascular regulatory mechanisms. An awareness about
the risk factors and identifying those patients who might stumble into a
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risk may significantly improve cardiovascular stability during dialysis.
Among high-risk patients, monitoring and biofeedback of the
varioushemodynamic variables, together with an extensive use of
convection, can prevent theappearance of symptomatic hypotension and
help in averting its onset.
Prevention of Intradialytic hypotension:
Educating the patient should be the first consideration in preventing
hypotension. Restrictions of salt consumption should be emphasized so
that interdialytic weight gain is limited to 3%. In addition other parameters
to be listed are
- Anaemia correction
- Patient end strategy
- Dietary and treatment compliance
- Avoid anti-hypertensive medication on the morning of the dialysis
day
- Avoid missing dialysis and stay the entire dialysis time for treatment
- Avoid eating during dialysis
Procedure related strategy:
Dialysate sodium- sodium profiling and sodium gradient protocol
but maintaining zerosodium balance to the possible extent.Approach to
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reduce the risk of Hypotension by approximating the dialysate Sodium
with endogenous sodium [9].Modelling fluid removal- sequential
ultrafiltration and dialysis, blood volume controlledhemodialysis. Cool
dialysate- isothermic dialysis is well tolerated and clearly reduces the
incidenceof hypotension. Reduction of the ultrafiltration rate with
prolongation of treatment time, Accurate estimation of dry weight
(segmental bio impedance, and others), Judiciously increasing dialysate
calcium while avoiding hypercalcemia are other measures that aid the
prevention of hypotension.
Treatment:
Stop or reduce ultrafiltration, Place patient in Trendelenburg
position. Administration of saline and hypertonic agents. Additional
dialysis sessions should be considered in patients gaining weight more than
3%. However, excess fluid replacementshould be avoided to prevent
sodium overload.Continuous infusion of pressor agents (meteraminol,
norepinephrine) are very rarelyneeded.
Midodrine an alpha 1 agonist given approximately 30 min before dialysis
significantly reduces theincidence of hypotension. It has been considered
safe and is well tolerated.It is initially started at a dose of 2.5 mg and then
titrated to a maximum of 30 mg.
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Carnitine has been recommended in-patients with frequent
hypotensiveepisodes.It acts by carrying long chain fatty acids to
mitochondria Given as intravenous administration of 20mg/kg during each
session. Sertraline,an SSRI in doses of 50 to 100mg per day decreases
intradialytic hypotension
INTRADIALYTIC HYPERTENSION
Most proposed mechanism for intradialytic hypertension is a state of
salt and volume excess. Other mechanisms include increased sympathetic
activity, activation of renin angiotensin system, endothelial cell
dysfunction, vascular stiffness, erythropoietin stimulating agents,
hypercalcemia, hypokalemia and stoppage of anti-hypertensives during
dialysis .
Pre-dialysis Blood pressure target of 140/90 mmHg and post dialysis target
of 130/80 mmHg is recommended
Treatment and Prevention
Lifestyle modifications such as weight reduction, dietary
modification, sodium restriction, physical activity and abstinence from
alcohol consumption can reducesystolic blood pressure from 2-14 mm Hg.
Adjustment of target weight on a regular basis. Gradual reduction of
interdialyticweight gain over a few weeks using zero sodium balance, salt
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restriction, longerdialysis or extra dialysis sessions may yield a significant
benefit. Reducing erythropoeitin dose in patients with severe hypertension
and withholding anti-hypertensive medications on the day of dialysis.
Calcium channel blockers are non dialyzable and can safely be used as a
second line of treatment in patients with heart failure. Nephrectomy may
be considered resistant cases. Renal transplantation or conversion to
peritoneal dialysis can also be considered (PD) [10].
DIALYZER REACTIONS
Reactions attributed to the hemodialyzer are generally divided into two
types:
Type A - anaphylactoid reaction
Increased risk in patients with a history of atopy, high IgE levels,
eosinophilia andallergic reactions during dialysis
Type B - mild reaction
Diagnosis:Type A reaction are severe and rapid in onset, Rare (7.0 per
1000 patient year). Established by three major criteria or two major and
one minor criterion
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- Major criteria
Onset within 20 minutes of starting dialysis, dyspnea, burning/heat
sensation at the access site or throughout the body and angioedema.
- Minor criteria
Reproducible during subsequent dialysis when using the same type or
brand of dialyzer, urticaria, rhinorrhea or lacrimation, abdominal cramping,
and itching.
Etiology: Use of ethylene oxide (ETO) for sterilization of dialyzer and
polyacrylonitrilemembranes (PAN) membranes, especially AN69 in
patients on ACE-inhibitors
Type B reaction:Primary symptoms are chest and back pain, that occur in
20-40 minutes during the dialysis treatment.It disappears or lessens
dramatically during the subsequent hours of dialysis. Pathogenesis behind
type B reaction is not clear.There is a probable relation with complement
activation [11].
DISEQUILIBRIUM SYNDROME
Disequilibrium syndrome most commonly occurs during the first
few dialysis sessions, in elderly and pediatric patients, patients with pre-
existing CNS lesions (recent stroke, head trauma) or
conditionscharacterized by cerebral edema (malignant hypertension,
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hyponatremia, hepaticencephalopathy), high pre-dialysis BUN, severe
metabolic acidosis
Etiology: Cerebral edema resulting from urea removal from the
blood more rapidly than fromthe CSF and brain tissue results in
generation of urea osmotic gradient.It is responsible for water moving into
the brain cells.HD generates a CO2 gradient between plasma and CSF
lowering the pH in the CSFand brain tissue. This change promotes an
increase in brain cell osmolality due tothe rise in H+ concentration and the
in-situ generation of osmotic concentration (acid radicals fromprotein
metabolism) resulting in brain edema.
Treatment:Usually self-limited. However, for severe symptoms HD
should be stopped.If seizures occur, glucose, diazepam, phenytoin loading
followed by infusion of osmotically active agents in dialysate have been
tried- albumin, glycerol, mannitol).
Prevention: Identify high risk patients, reduce dialysis efficacy and limit
urea reduction to 30% (smaller dialyzer, decreasingblood flow, sequential
dialysis increasing dialysis time), however, a recent smallseries found
tolerance to higher urea reduction. Prophylactic administration of
osmotically active agents (mannitol, glucose, fructose)and using high
sodium dialysate, IV mannitol 20% at 50 ml/hr with intravenous diazepam
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is a simple way to prevent disequilibrium syndrome in high risk patients
[12].
CRAMPING
Etiology: Approximately 20% of dialysis sessions are accompanied by
muscle cramps, which are more pronounced in patients who require high
ultrafitration rates and arepossibly dialyzed below their dry weight. They
are presumably related to reduction in muscle perfusion that occur in
response to hypovolemia. Compensatoryvasoconstrictive responses may
shunt blood centrally during treatment, and couldplay a role in promoting
muscle cramps.
Changes in intra or extracellular balance of potassium and
concentration of ionizedcalcium can disturb neuromuscular transmission
and produce cramps.
Peripheral vascular disease, although common in dialysis patients,
may not beassociated with increased prevalence of intradialytic cramps
which confirms thatprocesses related to the dialytic treatment are
responsible for the cramps, Middle molecule named leptin that is increased
in HD patients. It has an association with intradialytic cramping episodes
[13].
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Differential Diagnosis:While the majority of cramps are associated with
dialysis treatment, the differentialdiagnosis is extensive and includes the
following conditions:
- Idiopathic cramps
- Contractures (occurring in conditions such as metabolic myopathies,
and thyroiddisease)
- Tetany (due to hypocalcemia or alkalosis)
- Dystonias (occupational cramps, anti-psychotic medications)
- Other leg problems such as restless leg syndromes and periodic leg
movements,must be distinguished from cramps
Treatment and Prevention: Many of the treatment strategies are similar to
those used to treat intradialytichypotension. Physical manoeuvres such as
massage of the calf muscles and dorsiflexion of the footare not very
helpful. Immediate treatment is to increase intravascular volume by
interrupting or slowingultrafiltration and administering saline, mannitol or
glucose. In addition to effecting an intravascular shift of water, hypertonic
solutions may directly improve blood flow to the muscles and use of
dialysate sodium, potassium or calcium modelling. The concept
ofindividualization of dialysate composition seems to be a good preventive
method.Careful reassessment of the dry weight, counseling the patient to
reduce interdialyticweight gain and using bicarbonate dialysis. L-
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Carnitine [14]. and Vitamin E [15]. administration may reduce the
incidence of cramping.
AIR EMBOLISM
Etiology:Can be venous or less commonly, arterial. Three vulnerable areas
of air entry in dialysis patients:
1. Between patient and blood pump, due to high negative pressure and
leaks inthe circuit of the segment
2. Air in the dialysate fluid (uncommon, mostly gets trapped in venous
chamber)
3. During central venous catheter insertion or removal. Upright body
position and hypovolemia, both by reducing venous pressure,
aresignificant contributing factors[16].
Treatment: Prevent further air entry by clamping and disconnecting
the circuit. Flat supine position may be better over traditionally
advocated left lateral (Duran’sposition) and Trendelenburg position.
Oxygen with FiO 100%, Hyperbaric oxygen (prevents cerebral
edema), use of Luer-lock syringes for blood draw from catheters.
Prevention: Test machine prior to use to ensure that the air detector alarm
system is workingeffectively. Catheter insertion or removal should be in a
head low position (insertion site 5 cmbelow right atrium). Patient can assist
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by holding their breath or doing a Valsalvamaneuver that will increase
central venous pressure.
HEMOLYSIS
Etiology:
1. Mechanical
2. High blood pump flow
3. Single-needle dialysis
4. Small gauge cannula
5. Kinked blood lines
6. High negative arterial pressure
7. Offset blood pump
8. Failure of rinsing
9. Hydrogen peroxide
10.Contamination with hypochlorite, formaldehyde
11.Priming error
12.Hypotonic saline
13.Dialysate error
14.Hyper or hypotonic dialysate
15.Overheated dialysate
16.Dialysate contamination
17.Chloramines
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18.Nitrates
19.Copper
Treatment:Stop blood pump, clamp venous bloodline and discard the
blood. Provide oxygen to the patient. Arrange for blood transfusion if
needed. Resume HD as soon as patient is stabilized, since hyperkalemia
accompanies
hemolysis.
Prevention:Test machine prior to use to ensure that the air detector alarm
system is workingeffectively. Avoid chemical contaminants that can
damage RBCs, oxidants such as chloramines, copper, zinc, reducing agents
such as formaldehyde, hypo or hypertonic dialysate, overheated dialysate,
small needles and highly negative arterial pressure alarms. Ensure correct
positioning of tubing in the roller pumps
CARDIAC ARRYTHMIAS
Risk factors
- Left ventricular hypertrophy
- Heart failure
- Ischemic heart disease
- Other factors: Age, respiratory failure, rapid reduction of extra-
cellular volume, electrolyte and acid-base derangement, cardiac and
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major vascular surgery, digoxin therapy, sympathetic dysfunction,
increased phosphate and PTH, high risk in those with reduced heart
rate variability and increased QT dispersion [17].
Diagnosis and Treatment
Monitor serum electrolytes, bicarbonate and glucose levels, ECG, oxygen,
IV fluids. May need to discontinue HD. Correct electrolyte disturbance
(especially potassium,calcium and magnesium). Cardioversion with AED
(automated external defibrillator) in case patient ishemodynamically
unstable and has a treatable rhythm. Digoxin can be used to control
ventricular rate in SVT.
Patients on digitalis might need increase of the dialysate potassium to 3-
3.5
mEq/L to prevent hypokalemia.Amiodarone can be used in usual dose for
ventricular arrhythmias. Intracellular shift of potassium can be minimized
by reducing dialysate glucose (from200 to 100 mg/dl), and when acid base
status permits, bicarbonate level.
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Prevention:
Avoidance of low hemoglobin levels and hypoxia during dialysis.
Maintenance ofoptimal calcium, phosphate and PTH levels and usage of
oxygen.
HAEMORRHAGE
Risk Factors:Platelet dysfunction, Ineffective platelet-vessel wall
interaction and heparin induced thrombocytopenia(HIT), use of anti-
coagulation during HD, co-morbid conditions, uncontrolled hypertension,
liver disease, sepsis, certain medication (especially anti-platelet drugs),
Access site kept covered, Venous needle falling out or catheter connection
disrupted (venous pressure may falltoo little to cause an alarm).
Risk Assessment:Very high - Active bleeding during HD, High -
Surgical/traumatic wound within 3 days, Low - Surgical/traumatic wound
> 7 days.
Diagnosis and Treatment:Screen for bleeding and activated clotting time,
prolonged bleeding time - cryoprecipitate, DDAVP or conjugated estrogen,
acutely prolonged PTT (heparin induced) - Protamine, FFP.
Prevention:Should never keep access site covered, review heparin dose,
strategy based on risk assessment, low risk - low dose conventional
heparin, low molecular weight heparin, very high/high risk - regional
-
28
anticoagulation with heparin and protamine, heparinfree dialysis, regional
citrate anticoagulation, Prostaglandin (PGI2), PD, alternative Methods to
Conventional Heparin for high-risk patients
HYPOXIA
During hemodialysis, PaO2 falls about 10-20 mmHg. This decrease has no
clinicalconsequences in patients with normal oxygen tension, but in
seriously ill patients withpredialysis hypoxemia, the drop in PaO2 can be
catastrophic.
Etiology:
Acetate dialysate (now obsolete). Can also be seen with use of bicarbonate
Dialysate. Acetate causes hypoxemia by at least two mechanisms:
- Increased oxygen consumption in the metabolism of acetate to
bicarbonate
- Intradialytic loss of CO2
- Rapid correction of chronic metabolic acidosis
- Bioincompatible membranes
- Activation of complement
Hypocapnea due to intradialytic loss of CO2 and adaptation to chronic
metabolicacidosis predisposes to periodic breathing and sleep apnea
syndrome (SAS). SAS is also a cause of hypoxia in HD patients. High
-
29
prevalence in HD patients (54-80%) and has both obstructive and
centralcomponents.Can alter autonomic responses and cause arrhythmias,
pulmonaryhypertension, and systemic hypertension.
Treatment and Prevention
Dialysis-induced hypoxemia can be attenuated by interventions that
increase the CO2 content of the dialysate either by direct administration or
by using bicarbonatebuffered dialysate. Use of biocompatible membranes
might be helpful in critically ill patients who may already have some
degree of pre-dialytic hypoxia, it isnecessary to increase the ventilated
volumes and/or the percentage of FiO2 improvement in SAS has been
reported with the use of prolonged dialysis such asnocturnal and daily
hemodialysis
PRURITIS
Etiology:
Common abnormalities in ESRD play a role in pathogenesis such as:
- Xerosis (dry skin)
- Peripheral neuropathy
- Hypercalcemia
- Hyperphosphatemia
- Hypermagnesemia
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30
- Zinc depletion
- Hypervitaminosis A
No correlation found between standard biochemical tests (blood urea
nitrogen,creatinine, calcium, phosphate, parathyroid hormone) and uremic
pruritus. Chronic inflammation might have a probable role. Relationship
between pruritus and type of dialyzer is not clear.
Treatment:
Empirical, individualized and often ineffective. Skin emollients, capsaicin,
H-1 receptor antagonist, phototherapy (UVB).
Newer drugs: Thalidomide, nicergoline, lidocain, mexiletine,
cholestyramine,cromolyn sodium and Gabapentin. Other modalities:
Acupuncture, electric needle stimulation and sauna, parathyroidectomy and
renal transplantation in recalcitrant cases
Prevention:
Optimizing calcium, phosphate, magnesium, PTH and delivered dose of
dialysis(greatly reduced at Kt/V > 1.5 ). Avoidance of dialysis related
factors such as iodine, ethylene oxide. Find out any allergy to heparin.
Biocompatible membrane can be used preferably. Parathyroidectomy is
also considered for treatment. Renal transplantation is the only definitive
treatment
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31
FEBRILE REACTIONS
Febrile reactions are defined as a rise in temperature during HD of at least
0.5° C or arectal or axillary temperature during dialysis of at least 38.0 or
37.5° C respectively .Themajority (70%) of febrile reactions are associated
with pre-existing infections (vascularaccess, urinary and respiratory) .
HD related febrile reactions can be associated with localized infection of
the vascularaccess site (especially catheters and grafts) or products from
the dialysate and/or theapparatus used for HD treatment
Diagnosis and Treatment:
- Obtain blood cultures
- Begin broad spectrum antibiotics immediately
- Treatment largely supportive and empirical
- Cluster of similar cases should prompt a review of:
1. Water used for reprocessing dialysate
2. Processing procedure
3. Bicarbonate system
Prevention:
- Reduce the use of catheters for HD
- Reduce the susceptibility to infections by:
- Provide adequate HD
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32
- Prevent and/or treat malnutrition
- Optimize hemoglobin concentration
- Avoid iron overload
- Use biocompatible dialysis membrane
- Reduce S. aureus infections by screening nasal carriers and treating
with mupirocin.
METABOLIC ACIDOSIS
Can occur accidentally as a consequence of dialysate fluid containing
improper ratiosof acid and base concentrates in the form of acetate or
bicarbonate. Develops as a result of the accidental use of an acidic
concentrate instead ofacetate or bicarbonate and due to computer software
malfunction of the machine. Severe metabolic acidosis has been reported
during first 2 hours of HD using sorbentregenerative hemodialysis in
mechanically ventilated patients
Treatment: consists of intravenous administration of bicarbonate and
dialysis withbicarbonate dialysate of a correct concentration (38-40
mEq/L)
The mainstay of prevention is to fit all HD machines with a pH meter and
alarms thatwill prevent the extreme acid load, which may be caused by an
inappropriatelyprepared bicarbonate dialysate. Conductivity checks are
vital.
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33
METABOLIC ALKALOSIS
The most common cause is the loss of hydrochloric acid as a result of
vomiting ornasogastric suction.
Less common causes:Technical errors during HD, Malfunction of the
dialysis machine’s pH monitor and proportioning system (thereversed
connection of bicarbonate and acid concentrate containers to the entry
ports)
Severe metabolic alkalosis may cause:
- Tissue hypoxia
- Arrhythmia
- Seizure
- Delirium
- Stupor
Applying HD therapy with specially formulated low-bicarbonate, low-
acetate, or aciddialyses are safe and effective intervention for severe
metabolic alkalosis. Severemetabolic alkalosis can be corrected rapidly and
safely with bicarbonate concentratesdialysate between 25-28 mEq/L .
HYPOKALEMIA
Severe intradialytic hypokalemia can occur even when the dialysate
contains ahigher potassium concentration than the predialysis serum
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34
potassium concentration. The cause of the hypokalemia is a rapid shift of
potassium from the extracellular tothe intracellular space secondary to
correction of acidosis
Dialysis induced hyperkalemia is rare.
Reported causes of hypokalemia include:
- History suggesting prolonged potassium loss
- Marked acidosis
- Baseline moderate hypokalemia
Prevention and Treatment
Excess potassium removal during HD can prolong QTc interval on ECG
preferentiallyand predispose to arrhythmia. Try to keep post dialysis serum
potassium 2-3 mEq/L. Use dialysate with 3.0 mEq/l of potassium in
patients with CAD and/or on digoxin,unless there is chronic, severe
hyperkalemia. Never use 0 mEq/L potassium dialysate. Use of very low
dialysate potassium (1mEq/L) should be discouraged.
HYPERKALEMIA
Common in ESRD (around 10% of HD patients).Contributes to 3-5% of
deaths [18].
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35
Etiology:
- Excessive dietary potassium intake
- Metabolic acidosis
- Acute infection with marked catabolism
- Rhabdomyolysis
- Mineralocorticoid deficiency
- Medications
- Dialysis induced hyperkalemia (rare)
- High dialysate potassium concentration
- Haemolysis
HYPERNATREMIA
Hypernatremia can occur when sodium concentration is high and the
conductivitymonitors of the dialysis machine are not functioning or the
alarms are not set properly. Dialysate conductivity can be incorrectly
sensed as low by the coated conductivitycells (that gets coated by granules
from less soluble batch of sodium bicarbonatepowder). At the start of
dialysis if an error is made when connecting concentratecontainers. Also
occur during dialysis if containers run dry and conductivity monitor fail
[19].
-
36
Treatment:
Dialysis can be resumed with dialysate sodium 2 mEq/L lower than
plasma sodiumconcentration while infusing isotonic saline. Use of
dialysate sodium 3-5 mEq/L lowerthan plasma sodium might increase the
risk of disequilibrium syndrome.
Prevention:
Frequent check of conductivity monitors which can get coated with
bicarbonategranules and can cause falsely low readings.
HYPONATREMIA
Hyponatremia can occur at the start of dialysis if an error is made when
connecting concentratecontainers. During dialysis if containers run dry and
conductivity monitor fails [20].
Treatment:
- Clamp the bloodlines
- Discard the blood present in the dialysis tubing (as acute
hyponatremia during HD isfrequently associated with hemolysis and
hyperkalemia)
- Anticonvulsants and blood transfusion may be needed
Rapid correction of hyponatremia in HD patients may not be dangerous
(except forone case report )
-
37
Current recommendation would be to correct hyponatremia using the
guidelinescurrently accepted for nonuremic patients
Prevention:
Dialysate sodium level should be higher than that in plasma.
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38
MATERIALS AND METHODS:
Type of Study: Prospective observational study
Study population and period : Patients admitted in hemodialysis unit,
Tirunelveli Medical College and Hospital from the period of January 2017
to December 2017.
Sample size: 190 patients.
Inclusion criteria:
1. Patients over 13 years of age
2. Patients with Chronic Kidney Disease (CKD)
3. Acute Kidney Injury (AKI) were selected.
Exclusion Criteria:
1. Pregnant women
2. Patients below 13 years of age.
Methodology: The study was approved by ethical committee of the
Hospital. Non probability consecutive technique was used. The first
190 consecutive patients diagnosed with ARF and CKD were admitted in
hemodialysis unit from January 2017 to December 2017, who met within
the inclusion criteria were recruited for the study.
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39
After obtaining informed consent, patients were monitored and evaluated
thoroughly in recording the intradialytic complications with hemodialysis.
Incidence of complications with patients undergoing hemodialysis, most
common type of complications and how to treat such complications were
analysed.
-
40
STUDY ANALYSIS:
Statistical assessment was performed using chi-square analysis with
continuity correction and students t-test to identify the difference between
patient with and without intradialytic complications. Statistical
significance was assumed when the probability value was less than 0.05.
Data was analysed using SPSS-11. Data was expressed as mean 2SD and
percentage
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41
OBSERVATION AND RESULTS:
Table -1 : AGE WISE DISTRIBUTION OF PATIENTS ON HD
We included 190 total patients who are above 13 years of age.
S.No AGE IN YEARS NO OF PATIENTS PERCENTAGE
1 < 30 72 38%
2 31-40 74 39%
3 41-50 29 15%
4 51-60 8 4%
5 >60 7 4%
Figure -1 : AGE WISE DISTRIBUTION OF PATIENTS ON HD
Among our patients for hemodialysis, 31 to 40 years of age groups
constituted 39% and >60 Years was only 4%.
38%
39%
15%
4%4%
AGE DISTRIBUTION
< 30
31-40
41-50
51-60
>60
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42
Table-2 : SEX WISE DISTRIBUTION OF PATIENTS ON HD
S.No SEX NO OF PATIENTS PERCENTAGE
1 MALE 131 69%
2 FEMALE 59 31%
Figure -2 : SEX WISE DISTRIBUTION OF PATIENTS ON HD
Out of 190 patients, 69% were Male patientsand 31% were females.
69%
31%
SEX DISTRIBUTION
MALE
FEMALE
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43
Table-3 PREVALENCE OF ACUTE AND CHRONIC KIDNEY
DISEASE
S.NoDIAGNOSIS
NO OF
PATIENTS
PERCENTAG
E
1 CHRONIC KIDNEY
DISEASE175 92%
2 ACUTE KIDNEY
INJURY15 8%
Figure -3 PREVALENCE OF ACUTE AND CHRONIC KIDNEY
DISEASE
Out of 190 patients, CKD patients were more than AKI (CKD-92%)
92%
8%
DIAGNOSIS
CHRONIC KIDNEY DISEASE
ACUTE KIDNEY INJURY
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44
Table-4 DISTRIBUTION OF PATIENTS ON HD WITHCATHETER IN SITU
S.No CATHETER NO OF PATIENTS PERCENTAGE
1 PERMANENT 155 82%
2 TEMPORARY 35 18%
Figure -4 DISTRIBUTION OF PATIENTS ON HD WITH
CATHETER IN SITU
Among the 190 patients, patients with permanent catheter were more than
temporarily catheterised patients (permanent catheter-82%)
82%
18%
CATHETER
PERMENANT
TEMPORARY
-
45
Table-5 HEPATITIS C POSITIVITY IN HD PATIENTS
HEPATITIS C NO OF PATIENTS PERCENTAGE
POSITIVE 3 2%
NEGATIVE 187 98%
COMPLICATIONS Nil Nil
Figure -5 HEPATITIS C POSITIVITY IN HD PATIENTS
2% of patients were confirmed to be positive with hepatitis C, no specific
complications in HCV infected individuals.
2%
98%
HEPATITIS C
POSITIVE
NEGATIVE
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46
Table-6 SYSTOLIC BP –BEFORE DIALYSIS
S.No SYSTOLIC BP - BEFORE
DIALYSIS
NO OF
PATIENTS
PERCENTAG
E
1 MORE THAN 140mmhg 155 82%
2 LESS THAN 140mmhg 35 18%
Figure -6 SYSTOLIC BP –BEFORE DIALYSIS
82% of the patients were hypertensive. Among the 190 Patients 155
patients Blood pressure were more than 140mmHg.
82%
18%
SYSTOLIC BP - BEFORE DIALYSIS
MORE THAN 140
LESS THAN 140
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47
Table-7 SYSTOLIC BP – AFTER DIALYSIS
S.No SYSTOLIC BP - AFTER
DIALYSIS
NO OF
PATIENTS
PERCENTAG
E
1 MORE THAN 140mmhg 152 82%
2 LESS THAN 140mmhg 38 18%
FIGURE -7 SYSTOLIC BP – AFTER DIALYSIS
Post-hemodialysis, the blood pressure raise above normal stayed in 82%
SYSTOLIC BP AFTER DIALYSIS
MORE THAN 140 LESS THAN 140
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48
Table-8 COMPARISON OF SYSTOLIC BP BEFORE AND AFTER
HEMODIALYSIS
S.No SYSTOLIC BP BEFORE AFTER
1 MORE THAN 140mmhg 155(82%) 152(82%)
2 LESS THAN 140mmhg 35(18%) 38(18%)
Figure -8 COMPARISON OF SYSTOLIC BP BEFORE AND AFTER
HEMODIALYSIS
Patients with systolic pressure before and after the hemodialysis sessions.
155
35
152
38
M O R E T H A N 1 4 0 L E S S T H A N 1 4 0
SYSTOLIC BPBEFORE AFTER
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49
Table-9 DIASTOLIC BP – BEFORE DIALYSIS
S.No DIASTOLIC BP - BEFORE
DIALYSIS
NO OF
PATIENTS
PERCENTA
GE
1 MORE THAN 90mmhg 163 86%
2 LESS THAN 90mmhg 27 14%
Figure -9 DIASTOLIC BP – BEFORE DIALYSIS
Diastolic pressure before dialysis were higher than normal in 86% of the
patients
86%
14%
DIASTOLIC BP - BEFORE DIALYSIS
MORE THAN 90
LESS THAN 90
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50
Table-10 DIASTOLIC BP AFTER DIALYSIS
S.No DIASTOLIC BP - AFTER
DIALYSIS
NO OF
PATIENTS
PERCENTAG
E
1 MORE THAN 90mmhg 33 17%
2 LESS THAN 90mmhg 157 83%
Figure -10 DIASTOLIC BP AFTER DIALYSIS
Interestingly, diastolic pressure had a fall below 90mm Hg in 83% of the
patients
33
157
DIASTOLIC BP -AFTER DIALYSIS
MORE THAN 90 LESS THAN 90
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51
Table-11 COMPARISON OF DIASTOLIC BP BEFORE AND
AFTER HD
S.No DIASTOLIC BP BEFORE AFTER
1 MORE THAN 90mmhg 163(86%) 33(17%)
2 LESS THAN 90mmg 27(14%) 157(83%)
Figure -11 COMPARISON OF DIASTOLIC BP BEFORE AND
AFTER HD
A significant difference in diastolic pressure was recorded before and after
hemodialysis
163
3327
157
B E F O R E A F T E R
DIASTOLIC BPMORE THAN 90 LESS THAN 90
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52
Table-12 PATTERN OF DISTRIBUTION OF COMLICATIONS
WITH NUMBER OF SESSIONS OF HD
S.
No
NO OF SESSION OF
DIALYSIS
NO OF
PATIENTS
PERCENTAG
E
1 LESS THAN 50 137 72%
2 51-100 30 16%
3 MORE THAN 100 23 12%
Figure -12 PATTERN OF DISTRIBUTION OF COMLICATIONS
WITH NUMBER OF SESSIONS OF HD
Number of sessions of hemodialysis within our patient group. 72% of
patients underwent hemodialysis less than 50 times
72%
16%
12%
NUMBER OF SESSIONS DIALYSIS
LESS THAN 50
51-100
MORE THAN 100
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53
Table-13 COMPLICATIONS IN AKI
S.N
o
COMPLICATIONS OF
AKI(N=15)
NO OF
PATIENTS
PERCENTA
GE
1 PRESENT 9 60%
2 ABSENT 6 40%
Figure -13 COMPLICATIONS IN AKI
Among 15 patients 9 (60%) patients developed complications
9
6
0
1
2
3
4
5
6
7
8
9
10
PRESENT ABSENT
COMPLICATIONS IN AKI
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54
TABLE 14: CAUSES OF AKI
S.N
oCOMPLICATIONS
NO OF
PATIENTS
PERCENTAG
E
1 SNAKE BITE 6 40%
2 PARAQUAT POISONING 3 20%
3 HYDROURETERONEPHRO
SIS2 13%
4 RAPID PROGRESSIVE GN 2 13%
5 ACUTE PANCREATITIS 1 7%
6 OBSTRUCTIVE UROPATHY 1 7%
Figure-14 : CAUSES OF AKI
Among the 15 AKI patients 6 (40%) is due to snake bite and 20% Due to
paraquat poisoning.
40%
20%
13%
7%
13%7%
CAUSES OF AKI
SNAKE BITE
PARAQUAT POISONING
HYDROURETERONEPHROSIS
ACUTE PANCREATITIS
RAPID PROGRESSIVE GN
OBSTRUCTIVE UROPATHY
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55
Table-15 PREVALENCE OF COMPLICATIONS DURING HD
Sl.No COMPLICATIONS NO OF PATIENTS PERCENTAGE
1 PRESENT 64 34%
2 ABSENT 126 66%
Figure -15 PREVALENCE OF COMPLICATIONS DURING HD
34% of the patients were recorded with complications during
hemodialysis.
64
126
P R E S E N T A B S E N T
COMPLICATIONS
-
56
Table-16 PATTERN OF VARIOUS COMPLICATIONS
ENCOUNTERED DURING HD
Sl.N
oCOMPLICATIONS(N=64)
NO OF
PATIENTS
PERCENTAG
E
1. CRAMPS 18 28%
2. HYPOTENSION 16 25%
3. RIGOR 16 25%
4. CHEST PAIN 6 9%
5. FEVER 2 3%
6. HYPOGLYCEMIA 2 3%
7. VOMITING 2 3%
8. PALPITATION 1 2%
9. ACUTE PULMONARY
EDEMA1 2%
Among the complications 28 % were due to muscle cramping and 25%
each due to hypotension and rigors
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57
Figure -16 PATTERN OF VARIOUS COMPLICATIONS
ENCOUNTERED DURING HD
Various intradialytic complications of HD, 28% due to cramping and 25%
due to hypotension and another 25% due to rigors. These are the most
commonly encountered complications during intradialytic period.
28%
25%25%
9%3%3%
3%2%2%
COMPLICATIONS
CRAMPS
RIGOR
HYPOTENSION
CHEST PAIN
FEVER
HYPOGLYCEMIA
VOMITTING
PALPITATION
ACUTE PULMONARY EDEMA
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58
Table-17 COMPLICATIONS VS AGE IN YEARS
COMPLICATIONSAGE IN YEARS
MEAN SD
PRESENT 33.62 12.05
ABSENT 35.11 11.12
UNPAIRED T TEST
P VALUE - 0.411
NON SIGNIFICANT
Figure -17 COMPLICATIONS VS AGE IN YEARS
No significant relationship between age and intradialytic complications
noted within our study, probably because more number of patients were
between the age groups of 21 to 30 years
33.6
2
35.1
1
P R E S E N T A B S E N T
COMPLICATION VS AGE
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59
Table 18 COMPLICATIONS VS SEX
COMPLICATIONSSEX
MALE FEMALE
PRESENT 43(33%) 21(36%)
ABSENT 88(67%) 38(64%)
CHI SQUARE TEST
P VALUE - 0.709
NON SIGNIFICANT
Figure 18 COMPLICATIONS VS SEX
No significant relationship between gender and complication
43
21
88
38
M A L E F E M A L E
S E X
COMPLICATIONS VS SEXPRESENT ABSENT
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60
Table-19 COMPLICATIONS VS DIAGNOSIS
COMPLICATIONSDIAGNOSIS
CKD AKI
PRESENT 55(31%) 9(60%)
ABSENT 120(69%) 6(40%)
CHI SQUARE TEST
P VALUE - 0.025
SIGNIFICANT
Figure -19 COMPLICATIONS VS DIAGNOSIS
There is a significant relationship between intradialytic complications in
patients with AKI (60%)
55
9
120
6
0
20
40
60
80
100
120
140
CKD AKI
DIAGNOSIS
COMPLICATION VS DIAGNOSIS
PRESENT ABSENT
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61
Table-20 COMPLICATIONS VS CATHETER
COMPLICATIONSCATHETAR
PERMENANT TEMPORARY
PRESENT 49(31%) 15(43%)
ABSENT 106(69%) 20(57%)
CHI SQUARE TEST
P VALUE - 0.204
NON SIGNIFICANT
Figure -20 COMPLICATIONS VS CATHETER
Figure-20
No significance noted with the type of catheter and intradialytic
complication
49
15
106
20
PERMENANT TEMPORARY
CATHETAR
COMPLICATION VS CATHETER
PRESENT ABSENT
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62
Table-21 COMPLICATIONS VS BLOOD UREA
COMPLICATIONSBLOOD UREA
MEAN SD
PRESENT 168.23 55.32
ABSENT 146.7 51.97
UNPAIRED T TEST
P VALUE - 0.024
SIGNIFICANT
Figure -21 COMPLICATIONS VS BLOOD UREA
There is a significant statistical correlation between blood urea levels and
intradialytic complications.
168.
23
146.
7
P R E S E N T A B S E N T
MEAN UREA VS COMPLICATIONS
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63
Table 22 COMPLICATIONS VS SERUM CREATININE
COMPLICATIONSSERUM CREATININE
MEAN SD
PRESENT 13.69 4.44
ABSENT 10.13 4.72
UNPAIRED T TEST
P VALUE - 0.036
SIGNIFICANT
Figure 22 COMPLICATIONS VS SERUM CREATININE
There is a noted statistical significance between serum creatinine levels
and intradialytic complications.
13.69
10.13
0
2
4
6
8
10
12
14
16
PRESENT ABSENT
MEAN CREATININE VS COMPLICATIONS
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64
Table – 23 COMPLICATION VS POTASSIUM LEVELS
COMPLICATIONSPOTASSIUM
MEAN SD
PRESENT 5.23 0.73
ABSENT 4.72 0.77
UNPAIRED T TEST
P VALUE - 0.05
SIGNIFICANT
Figure – 23 COMPLICATION VS POTASSIUM LEVELS
Statistical significance noted with Potassium levels and Intradialytic
complications
4.44.54.64.74.84.9
55.15.25.3
PRESENT ABSENT
5.23
4.72
MEAN POTASSIUM VSCOMPLICATIONS
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65
Table-24 COMPLICATION VS NUMBER OF SESSIONS OF
DIALYSIS
COMPLICATIONSNO OF SESSIONS
MEAN SD
PRESENT 38.98 48.67
ABSENT 53.73 65.01
UNPAIRED T TEST
P VALUE - 0.111
NON SIGNIFICANT
Figure -24 COMPLICATION VS NUMBER OF SESSIONS OF
DIALYSIS
No significant correlation between number of sessions and intradialytic
complications noted
38.9
8
53.7
3
P R E S E N T A B S E N T
NO OF SESSIONS VS COMPLICATIONS
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66
Table-25 COMPLICATION VS SYSTOLIC BP BEFORE DIALYSIS
COMPLICATIONSSYSTOLIC BP -BEFORE DIALYSIS
MEAN SD
PRESENT 144.21 22.45
ABSENT 152.36 21.7
UNPAIRED T TEST
P VALUE - 0.017
SIGNIFICANT
Figure -25 COMPLICATION VS SYSTOLIC BP BEFORE
DIALYSIS
There is a significant relationship with complications and high systolic
blood pressure before dialysis
144.
21
152.
36
P R E S E N T A B S E N T
SYSTOLIC BP- BEFORE DIALYSIS VSCOMPLICATION
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67
Table-26 COMPLICATION VS SYSTOLIC BP AFTER DIALYSIS
COMPLICATIONSSYSTOLIC BP - AFTER DIALYSIS
MEAN SD
PRESENT 131.4 33.15
ABSENT 147.54 20.02
UNPAIRED T TEST
P VALUE - 0.001
SIGNIFICANT
Figure -26 COMPLICATION VS SYSTOLIC BP AFTER DIALYSIS
Statistical significance noted in systolic BP before and after hemodialysis
versus complications
131.4
147.54
120 125 130 135 140 145 150
PRESENT
ABSENT
SYSTOLIC BP -AFTER DIALYSIS VSCOMPLICATIONS
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68
Table-27 COMPLICATION VS DIASTOLIC BP BEFOREDIALYSIS
COMPLICATIONSDIASTOLIC BP -BEFORE DIALYSIS
MEAN SD
PRESENT 87.03 10.18
ABSENT 91.34 9.91
UNPAIRED T TEST
P VALUE - 0.001
SIGNIFICANT
Figure -27 COMPLICATION VS DIASTOLIC BP BEFOREDIALYSIS
There is a significant relationship with diastolic blood pressure and
complications
87.03
91.34
84
85
86
87
88
89
90
91
92
PRESENT ABSENT
DIASTOLIC BP - BEFORE DIALYSIS
-
69
Table -28 COMPLICATION VS DIASTOLIC BP AFTER DIALYSIS
COMPLICATIONSDIASTOLIC BP - AFTER DIALYSIS
MEAN SD
PRESENT 79.68 18.08
ABSENT 89.12 9.12
UNPAIRED T TEST
P VALUE - 0.001
SIGNIFICANT
Figure -28 COMPLICATION VS DIASTOLIC BP AFTERDIALYSIS
There is also a statistical significance with diastolic BP before and after
versus intradialytic complications
79.6
8
89.1
2
P R E S E N T A B S E N T
DIASTOLIC BP AFTER DIALYSIS VSCOMPLICATIONS
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70
Table-29 Patients with pre-existing Hypertension in our group:
S.No Numbers Percentage
1 Patients with
HTN
163 86%
2 Patients without
HTN
27 14%
In our study out of 190 patients 163 Patients were Hypertensives
Table-30 Patients with Pre-existing DM in our group:
S.No Numbers Percentage
1 Patients with DM 20 11%
2 Patients without
DM
170 89%
In our study out of 190 patients 20 Patients were diabetic.
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71
Table-31 AGE WISE DISTRIBUTION OF MUSCLE CRAMPING
Sl.No Cramps Males Females
1 13-20 yrs 3 1
2 21-30 yrs 4 0
3 31-40 yrs 4 0
4 >40 Yrs 5 1
Cramping is a common complications associated with people undergoing
HD of >40 years of Age Group ,among the 18 patients 16 were males and
2 were females,cramping occurs in 34% in patients with age more than 40
years.Cramping is common compication in both CKD and AKI patients.
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72
Table-32 Age wise distribution of Hypotension
S.No Hypotension Males Females
1 13-20 yrs 1 0
2 21-30 yrs 3 1
3 31-40 yrs 2 4
4 >40 Yrs 4 1
Hypotension is also a common complication in old age group people. In
our study hypotension (25%) was the second most common complication
encountered during the process of HD. 38% were between 31 to 40 years
of age and 6% were 13 to 20 years of age group.
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73
Table-33 Percentage of Hypotensive occurrence in AKI and CKD
Complication AKI (15 patients) CKD (175 patients)
Hypotension(16 patients)
4 12
Percentage 27% 7%
Figure-29 Percentage of Hypotensive occurrence in AKI and CKD
Among the 15 AKI patients 4(27%) developed hypotension compared to
CKD 12(7%)
0
5
10
15
20
25
30
35
Hypotension
CKD
AKI
-
74
DISCUSSION:
Intradialytic complications are the major issues in patients with both
AKI and CKD, who get into the hemodialysis routine as a part of their
treatment.In our study the number of patients are more between the age
group of 31 and 40 years. Gender wise analysis showed male
preponderance(M:F 2.2:1) Hypotension (50%) is stated as the most
common complication of hemodialysis [21]. More number of patients in
our group who underwent hemodialysis had a prior diagnosis of CKD
(92%).
In our study, out of 190 patients 64 (34%) developed complications.
Among the 15 AKI patients, 9 (60%) developed complications compared
with 31.4%. in CKD patients. In the study by Prabakar et al [22]
hypotension was the most common complication with HD patients (20 to
50%). In another study by Mehimood et al [23] 37.5% developed
hypotension and 12.5% patients developed cramps. In our study, 18
patients (28%) developed cramps and 25% patients got hypotension as an
intradialytic complication. These 2 complications were the main
complication in our study in AKI and CKD patients. There is no significant
age and sex distribution relation in our study.There is no significant
relationship between HCV infection with complications.
-
75
Muscle cramps in 18 patients (28%) being the commonest complication in
our group might be due to excessive ultrafiltration and low dialysate
sodium percentage. The next common problem in our group of patients
were hypotension in 16 patients (25%) and rigors in 16 patients (25%).
Hypotension could be probably due to high dialysate temperature, anti-
hypertensive medication, high ultra-filtrate rate, autonomic dysfunction
and low dialysate sodium.
There is a significant relationship with hypertension and no
significant relationship with diabetes in our study. Other complications
developed during the intradialytic period are chest pain(9%), fever(3%),
hypoglycaemia(3%), vomiting(3%), palpitations(2%) and acute pulmonary
edema (2%).
Complications such as Haemorrhage, hemolysis and arrhythmias did
not occur on our study group of HD patients.
-
76
SUMMARY
Among 190 patients with renal failure who underwent hemodialysis,
they were selected strictly under inclusion criteria the following
were observed.
1. Males (69%) developed more complications than females
(31%).
2. Among 190 patients 92% were CKD patients and 8% had
AKI.
3. Among 190 patients 64 (34%) developed intradialytic
complications.
4. Patients with less than 50 sessions developed more
complications
5. Complications were more with AKI patients. Snake bite
was the common cause of AKI in our study.
6. Cramps and hypotension were the most common
complications in our study.
7. No relation with Hepatitis C infection and complication.
-
77
CONCLUSION
Hemodialysis is a better procedure for removal of toxic metabolic end
products from systems in renal failure patients, but associated with risks
with this 4 hour procedure. Thorough monitoring with each of the patient
who underwent hemodialysis, 34% patients developed intradialytic
complications and I am with this inference that, muscle cramps(28%),
hypotension (25%) and rigors (25%) occur commonly and necessary
precautionary measures has to be kept in line, if in case an emergency
occur. Chest pain (9%) , Fever(3%) , hypoglycaemia (3%), vomiting(3%) ,
palpitations (2%) and acute pulmonary oedema(2%) should also be sought
in mind to execute and emergency plan of action. In our study no
significant relationship between age and sex distribution with
complications.
-
BIBLIOGRAPHY
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venepuncture and a surgically created arteriovenous fistula. N Engl
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the planning of arteriovenous fistulas for hemodialysis. Semin Dial.
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7. Jesus AC, Oliveira HA, Paixoa MO, Fraga TP, Barreto FJ, Valenca
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Asthma Immunol;78:217-220
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Disequilibrium Syndrome by use of high Sodium concentration in
dialysis, 1973 Kidney Int;3:327-333
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14.Lynch KE, Feldman HI, Berlin JA,et al. Effects of L-carnitine on
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Am J Kidney Dis.2008;52:962-971
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nocturnal leg cramps? Consult Pharm.2008;23:141-156
16.Vesely TM et al, Air embolism during insertion of central venous
catheters, 2001, J VascIntervRadiol; 12 :1291-1295.
17.Erem C, Kulan K, Tuncer C, Bostan M, Mocan Z, Komsuoglu B et
al,Cardiac arrtythmia in patients on maintenance hemodialysis,
1997, Acta Cardiol;52:25-36
18.Ahmed J, Weisberg LS et al, Hyperkalemia in dialysis patients, 2001
Semin Dial;14:348-356
19.Sterna RH, Silver SM, et al,Hemodialysis in hyponatremia : is there
a risk? 1990, Semin Dial;3:3-4
20.Oliveno JJ, Dischosoc et al, Severe Hyponatremia in a home dialysis
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22.Prabhakar, Singh RG, Singh S, Rathore SS, Choudhary TA et al,
Spectrum of Intradialytic Complications during Hemodialysis and
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its Management: A single-Center Experience, Saudi J Kidney Dis
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et al. Intradialytic Complications found in patients at a Tertiary Care
Hospital. Austin J PharmacolTher. 2016; 4(1):1079
-
PROFORMA
Name :
Age/Sex :
Address :
Diagnosis : AKI/ CKD
Nature of the catheter : Permanent / Temporary
Number of Sessions:
Haemodialysis :
Starting Time
Ending Time
HCV : Positive / Negative
Symptoms:
Hypotension Yes / No
Nausea Yes / No
Vomiting Yes / No
Headache Yes / No
Fever Yes / No
Chills Yes / No
Muscle Cramps Yes / No
Chest Pain Yes / No
-
Itching Yes / No
Past History
Diabetes Mellitus
Hypertension
Family History
Positive / Negative
Investigations
Blood Sugar
Renal Function Test
Blood Urea
Serum Creatinine
Serum Electrolytes
Sodium
Potassium
ECG and X ray Chest (if Needed)
-
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gq;F ngWthpd; ngaH:
gq;F ngWthpd; taJ:
gq;F ngWth;
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mwpe;J nfhz;Nld;.
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4. ,e;j Ma;tpd; %yk; fpilf;Fk; jftiyNah> KbitNah gad;gLj;jpf; nfhs;s kWf;f khl;Nld;.
5. ,e;j Ma;tpy; gq;F nfhs;s xg;Gf; nfhs;fpNwd; vdf;F nfhLf;fg;gl;lmwpTiufspd; gb ele;J nfhs;tJld;> Ma;it
Nkw;nfhs;Sk; kUj;Jt mzpf;F cz;ikAld; ,Ug;Ngd; vd;W
cWjpaspf;fpNwd;. vd; cly; eyk; ghjpf;fg;gl;lhNyh> my;yJ
vjpHghuhj> tof;fj;jpw;F khwhd Neha;Fwp njd;gl;lhNyh clNd
,ij kUj;Jt mzpaplk; njhptpg;Ngd; vd cWjp mspf;Nwd;.
gq;Nfw;gthpd; ifnahg;gk; / .................................................... ,lk; ...........................................
fl;iltpuy; Nuif
gq;Nfw;gthpd; ngaH kw;Wk; tpyhrk; ........................................................................................
Ma;thshpd; ifnahg;gk; /...................................................... ,lk; ............................................
Ma;thshpd; ngaH .........................................................................................................................
ikak; ...............................................................................................................................................
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rhl;rpapd; ifnahg;gk; /...................................................... ,lk; ................................................
ngaH kw;Wk; tpyhrk; ................. ...................................................................................................
-
S.no Ag
e
Diag
nosi
s
HHH
Ure
a
Crea
tinin
e
Na K
No
of S
essi
ons
DM HTN
Caus
e
INTR
ADIL
AYTI
CCO
MPL
ICAT
ION
S
M FPERMANENT
TEMPORAR
YBefore DIALYSIS
AfterDIALYSIS
1 38 1 ckd 1 neg 183 13.7 140 4.6 9 1 160/100 90/70 Hypotension2 37 1 ckd 1 neg 111 9.1 136 5.3 18 1 140/100 140/90 nil3 38 1 ckd 1 neg 148 12.4 150 5.8 24 1 190/100 180/90 rigor4 25 1 ckd 1 neg 230 9.7 128 5.1 40 1 180/100 140/80 nil5 32 1 ckd 1 neg 98 13.8 136 4.9 50 1 150/100 150/100 nil6 41 1 ckd 1 neg 124 11.1 142 5.8 4 1 1 190/100 100/60 hypotension7 30 1 ckd 1 neg 88 9 145 4.2 23 1 160/100 180/90 nil8 20 1 ckd 1 neg 180 13.6 128 4 17 1 150/90 140/80 cramps9 57 1 ckd 1 neg 103 11 140 5.4 12 1 1 160/100 180/90 nil10 26 1 aki 1 neg 260 8.9 136 4.9 1 1 140/90 130/90 RPGN cramps11 50 1 ckd 1 neg 144 9.3 143 5.3 16 1 1 190/100 180/90 nil12 31 1 ckd 1 neg 196 12 140 6.3 4 1 140/90 150/90 chest pain13 25 1 ckd 1 neg 120 9 137 5.4 36 1 150/90 100/70 nil14 56 1 ckd 1 neg 189 13.2 152 5.2 65 1 1 190/100 190/100 nil15 37 1 ckd 1 neg 148 10.7 130 6 47 1 150/100 140/90 nil16 36 1 ckd 1 neg 120 9.7 152 5.2 23 1 140/90 140/90 nil17 31 1 ckd 1 neg 189 14.6 142 5.5 43 1 150/90 160/90 hypoglycemia18 40 1 ckd 1 neg 140 9.8 129 4.4 22 1 160/100 110/80 rigors19 37 1 ckd 1 neg 112 9.2 137 5.9 27 1 140/90 150/100 nil20 48 1 ckd 1 neg 120 9.8 138 5 29 1 1 150/100 140/90 nil21 39 1 ckd 1 neg 130 11 132 4.2 38 1 150/90 110/80 rigors22 25 1 ckd 1 neg 128 14 145 5.8 4 1 190/100 180/90 nil23 29 1 ckd 1 neg 141 10.4 136 4.6 1 1 140/100 100/70 cramps24 31 1 ckd 1 neg 198 12.1 123 4.2 15 1 180/90 160/90 nil25 50 1 ckd 1 neg 92 11 141 5.8 19 1 1 150/100 150/100 nil26 31 1 ckd 1 neg 68 9.6 132 5 18 1 120/90 90/60 hypotension27 37 1 ckd 1 neg 168 11 152 4.6 2 1 140/90 140/80 nil28 22 1 ckd 1 neg 300 18.2 127 4.9 45 1 150/100 140/90 nil29 45 1 aki 1 neg 260 10.2 138 5.9 2 1 1 180/90 160/90 RPGN nil30 25 1 ckd 1 neg 194 12.6 138 5 50 1 150/100 140/90 nil31 31 1 ckd 1 neg 226 26 128 3.6 23 1 180/100 180/90 cramps
BLO
OD
PRES
SURE
Cath
eter
Gend
er
-
32 30 1 ckd 1 neg 141 8.8 139 4.8 13 1 140/90 140/80 nil33 47 1 ckd 1 neg 98 9.4 140 4 49 1 1 120/90 120/80 nil34 16 1 ckd 1 neg 146 9.8 140 5 2 1 140/90 130/80 nil35 18 1 ckd 1 neg 230 12.1 120 4 19 1 180/100 170/90 nil36 25 1 ckd 1 neg 121 10.2 143 4.2 3 1 130/90 140/90 nil37 43 1 ckd 1 neg 112 11.6 128 4.5 26 1 140/90 90/60 hypotension38 25 1 ckd 1 neg 180 16 142 5.4 31 1 200/100 190/100 nil39 30 1 ckd 1 neg 160 12.6 143 4 18 1 140/100 140/90 nil40 34 1 ckd 1 neg 145 9 145 4.4 41 1 180/90 180/90 cramps41 34 1 ckd 1 neg 300 33.6 156 6 45 1 120/80 120/80 nil42 22 1 ckd 1 neg 149 14.9 132 3.1 23 1 150/100 140/90 nil43 48 1 ckd 1 neg 240 20 145 4.2 18 1 1 190/100 140/90 nil44 17 1 ckd 1 neg 160 9.4 128 6.2 8 1 160/90 160/80 nil45 36 1 ckd 1 neg 98 8.9 140 5.7 43 1 120/90 120/80 rigor46 30 1 ckd 1 neg 121 12.6 138 4 4 1 130/90 140/90 nil47 24 1 ckd 1 neg 200 21 135 5.4 36 1 140/90 150/90 nil48 37 1 ckd 1 neg 168 16 121 4.1 21 1 180/100 180/100 chest pain49 22 1 ckd 1 neg 140 4.2 2 1 140/90 140/90 nil
50 21 1 aki 1 neg 260 9.6 145 5.6 2 1 140/90 140/90snakebite
nil
51 25 1 ckd 1 neg 145 11 150 4.6 3 100/70 100/70 nil52 25 1 ckd 1 neg 96 9.3 142 4.7 30 1 180/100 160/100 rigor53 44 1 ckd 1 neg 154 12.6 120 4 24 1 1 160/100 140/90 nil54 19 1 ckd 1 neg 142 14.1 136 5 24 1 120/90 130/80 nil55 62 1 ckd 1 neg 300 33.4 140 6 25 1 1 190/100 180/90 cramps56 57 1 ckd 1 neg 160 12 150 5.4 12 1 130/90 100/80 nil57 20 1 ckd 1 neg 102 12.6 143 5.2 18 1 150/90 140/70 nil58 50 1 ckd 1 neg 164 9.6 136 4.8 41 1 170/90 150/90 chest pain59 38 1 ckd 1 neg 188 12.1 128 5.4 8 1 160/90 160/100 nil60 18 1 ckd 1 neg 144 8.6 135 4.9 24 1 140/90 120/80 nil
61 26 1 aki 1 neg 260 9 142 5.4 1 1 140/90 130/90snakebite
cramps
62 25 1 ckd 1 neg 152 14.3 140 4.6 2 130/80 90/40 hypotension63 34 1 ckd 1 neg 98 11.1 136 5 39 120/80 110/80 nil64 43 1 ckd 1 neg 106 12.6 132 6.4 30 1 180/100 170/90 nil65 30 1 ckd 1 neg 207 13.4 148 3 18 1 140/90 120/90 nil66 34 1 ckd 1 neg 220 17.8 141 5 37 1 160/90 150/100 fever67 24 1 ckd 1 neg 160 14.1 140 4.6 20 1 160/100 150/90 nil
-
68 36 1 ckd 1 neg 145 9.8 139 4.2 9 1 140/100 140/90 nil69 31 1 ckd 1 neg 126 10.6 127 4.1 8 1 150/100 150/100 rigors70 22 1 ckd 1 neg 107 15.7 136 3.8 3 1 160/100 160/90 vomiting71 37 1 ckd 1 neg 139 20.2 137 4.2 11 1 160/100 150/90 nil72 18 1 ckd 1 neg 125 12.7 141 4.5 14 1 150/90 120/80 cramps73 36 1 ckd 1 neg 211 18.6 140 6 3 1 160/90 150/90 nil74 25 1 ckd 1 neg 160 17.2 128 4 4 1 150/90 140/90 hypoglycemia75 62 1 ckd 1 neg 141 15.7 142 4.6 46 1 1 180/100 190/80 nil76 37 1 ckd 1 neg 120 10.6 138 4.5 43 1 130/90 130/90 nil77 36 1 ckd 1 neg 196 14.6 130 5 41 1 130/100 90/40 hypotension78 37 1 ckd 1 neg 140 7.8 140 6.2 23 1 160/90 150/100 nil
79 58 1 aki 1 neg 236 20.6 146 5.6 2 1 130/90 140/90B/L
HUNnil
80 48 1 Ckd 1 neg 120 9.6 142 4.2 24 1 160/90 150/90 nil81 33 1 Ckd 1 neg 152 14.2 138 4.5 26 1 180/90 160/100 nil82 32 1 ckd 1 neg 103 11 125 3 89 1 140/90 120/80 rigor83 39 1 ckd 1 neg 156 14 152 4.6 56 1 1 160/90 150/80 nil84 29 1 ckd 1 neg 165 11.2 136 4.1 106 1 130/90 140/90 cramps85 25 1 ckd 1 neg 146 12.1 142 3.8 67 1 140/90 140/90 nil86 36 1 ckd 1 neg 189 14.2 140 3.7 27 1 130/90 80/50 hypotension87 34 1 ckd 1 neg 98 9 141 4.5 16 1 140/90 120/80 nil88 36 1 ckd 1 neg 268 27 145 6.4 26 1 160/90 150/90 nil89 28 1 ckd 1 neg 144 14.6 142 4.1 103 1 140/90 140/90 cramps90 31 1 ckd 1 neg 156 12.2 144 4.2 230 1 160/100 150/90 nil91 18 1 ckd 1 neg 126 12 142 4.2 36 1 150/90 140/80 rigor92 25 1 ckd 1 neg 101 9.7 127 5 96 1 150/100 150/100 nil
93 40 1 aki 1 neg 286 26.7 126 5.7 2 1 100/70 80/50
AcutepancreatitiswithAKI
hypotension
94 32 1 ckd 1 neg 90 12.3 132 5.2 45 1 200/100 180/90 nil95 42 1 ckd 1 neg 200 22.6 143 6.4 95 1 180/100 180/90 nil96 34 1 ckd 1 neg 186 14.6 146 4.9 236 1 160/90 150/100 cramps97 22 1 ckd 1 neg 147 16.2 130 4.9 42 1 130/90 120/80 nil98 17 1 ckd 1 neg 159 12.7 142 5.6 4 100/70 100/80 vomiting99 24 1 ckd 1 neg 212 30 140 7.1 87 1 130/90 140/80 nil100 18 1 ckd 1 neg 178 12.1 138 5 47 1 140/90 150/100 rigor
-
101 62 1 ckd 1 neg 190 17.6 151 5.4 41 1 1 180/100 160/90 nil102 19 1 ckd 1 neg 106 14.5 140 5.6 7 1 140/100 150/90 cramps103 44 1 ckd 1 neg 96 9 138 4.7 78 1 160/90 140/80 nil104 39 1 ckd 1 neg 236 13.6 139 4.1 18 120/80 80/40 hypotension105 37 1 ckd 1 neg 178 17 142 5.7 27 120/80 110/80 nil106 32 1 ckd 1 neg 89 20.1 125 4.8 326 1 160/100 160/90 nil107 50 1 ckd 1 neg 122 16.9 153 6 56 1 170/100 180/100 rigor108 39 1 ckd 1 neg 112 17.1 138 6.4 79 170/80 170/90 nil109 29 1 ckd 1 neg 80 16.3 148 5.2 88 160/80 160/100 fever110 50 1 ckd 1 neg 125 13.6 149 4.4 18 1 1 180/110 170/100 nil111 28 1 ckd 1 neg 178 17.6 138 4.1 205 1 190/100 180/90 rigors112 25 1 ckd 1 neg 163 14.2 152 5.7 72 1 170/100 170/100 nil113 38 1 ckd 1 neg 98 10.7 135 3.9 12 1 160/90 70/40 hypotension114 38 1 ckd 1 neg 302 27.8 146 5.6 7 1 1 160/110 170/110 nil115 38 1 ckd 1 neg 148 14.2 144 4.9 72 1 150/90 140/90 nil116 31 1 ckd 1 neg 139 12.4 140 4.1 27 1 150/100 150/90 chest pain117 32 1 ckd 1 neg 198 18.7 138 4.8 6 120/80 120/80 nil118 47 1 ckd 1 neg 104 12.7 140 5.8 78 1 148/90 150/90 nil
119 35 1 aki 1 neg 296 12.2 146 5.6 3 140/80 140/90snakebite
cramps
120 18 1 aki 1 neg 246 14.4 142 5.4 1 1 130/90 130/80paraq
uatcramps
121 19 1 ckd 1 neg 98 9.7 160 5.2 78 130/60 140/70 nil122 44 1 ckd 1 neg 121 12.7 141 4.7 104 1 150/100 150/90 nil123 40 1 ckd 1 neg 138 13.9 147 5.3 52 1 160/90 90/60 hypotension124 39 1 ckd 1 neg 140 12 141 4.2 16 1 180/100 180/90 nil125 32 1 ckd 1 neg 173 19.7 149 4.3 45 1 150/100 140/100 nil126 47 1 ckd 1 neg 127 14.8 128 3.2 12 130/80 140/90 nil127 50 1 ckd 1 neg 147 15.2 140 5.2 32 130/70 120/70 palpitations128 57 1 ckd 1 neg 170 17.3 142 4.8 4 1 200/100 190/110 nil129 38 1 ckd 1 neg 180 16.9 138 4 78 1 160/90 140/80 nil
130 61 1 aki 1 neg 252 18.6 145 5.6 2 1 140/90 150/80
Obstructive
uropathy
cramps
131 20 1 ckd 1 neg 139 20.2 143 5.4 167 1 200/120 160/80 nil132 50 1 ckd 1 neg 138 16.3 140 4.2 92 1 150/100 150/90 nil
-
133 32 1 ckd 1 neg 148 12.7 142 4.1 230 1 160/110 170/100 nil134 42 1 ckd 1 neg 220 20.7 148 4.5 78 1 150/100 150/90 nil135 31 1 Ckd 1 neg 188 16.8 141 5.8 106 120/80 120/80 nil136 34 1 ckd 1 neg 104 10.7 137 4.5 92 1 160/90 150/100 nil137 34 1 ckd 1 neg 98 9.2 130 4.4 4 1 140/90 70/50 hypotension138 22 1 ckd 1 neg 188 16.7 132 4.2 27 140/80 130/90 nil139 17 1 ckd 1 neg 141 14.2 148 6 186 1 160/90 140/80 nil140 48 1 ckd 1 neg 138 15.1 141 4.8 111 150/80 140/70 cramps141 37 1 ckd 1 neg 201 18.2 142 3.8 27 1 160/100 150/90 nil142 24 1 ckd 1 neg 188 12.7 143 3.5 11 130/80 170/120 nil
143 45 1 aki/cellulitis 1 neg 280 22.6 148 6.2 3 1 150/90 140/100snakebite
nil
144 36 1 ckd 1 neg 186 16.4 142 4.8 230 1 160/90 160/100 nil145 25 1 ckd 1 neg 156 14.4 147 4.4 4 140/80 140/90 nil146 62 1 ckd 1 neg 148 12.7 144 5.1 12 160/70 150/80 nil147 44 1 ckd 1 neg 203 18.7 138 4.3 203 1 160/90 160/80 nil148 40 1 ckd 1 neg 166 13.2 141 4.1 42 140/80 140/90 nil
149 26 1 aki 1 neg 146 9.6 140 4.4 1 1 140/90 90/60
Paraquat
poisoning
hypotension
150 39 1 ckd 1 neg 189 17.6 150 3.8 96 1 130/90 140/90 nil151 19 1 ckd 1 neg 100 12.3 130 4.8 6 1 140/90 140/90 nil152 37 1 ckd 1 neg 162 18 142 4 46 1 120/90 160/90 nil153 36 1 ckd 1 neg 230 18.2 148 5.4 205 1 170/100 170/100 nil154 34 1 ckd 1 neg 152 12.6 140 4.1 47 1 200/100 190/100 nil
155 22 1 aki 1 neg 230 12.6 142 4.7 2 1 140/100 140/90snakebite
rigors
156 48 1 ckd 1 neg 146 11.7 128 4.2 94 1 150/100 140/90 nil157 39 1 ckd 1 neg 158 14.2 143 5 41 1 180/100 170/100 nil158 59 1 ckd 1 neg 90 9.8 145 4.8 232 1 140/90 140/80 nil159 59 1 ckd 1 neg 152 13.2 140 5.2 23 1 160/90 160/90 nil160 25 1 ckd 1 neg 140 11.1 141 4.4 11 120/80 90/50 hypotension161 48 1 ckd 1 Neg 75 9.4 138 5.6 121 1 150/90 120/80 nil162 36 1 ckd 1 neg 113 10.8 141 5.4 125 1 160/90 180/100 nil163 28 1 ckd 1 neg 60 10 139 5.5 100 1 200/110 170/110 nil164 18 1 ckd 1 neg 87 15.3 141 5.8 90 1 150/90 180/100 rigor165 27 1 ckd 1 neg 118 17.6 141 6 138 150/70 160/100 chest pain
-
166 32 1 ckd 1 neg 93 13.3 141 5.6 56 1 160/90 160/90 nil167 48 1 ckd 1 neg 64 8.2 148 5.9 168 140/80 190/100 Ac Pul Oedema168 21 1 ckd 1 neg 87 9.3 138 5.6 42 1 150/90 140/100 nil169 36 1 ckd 1 neg 230 16.7 130 6.2 169 1 180/100 180/100 nil
170 25 1 aki 1 neg 68 6 148 5.2 1 120/80 130/80Snakebite
nil
171 32 1 ckd 1 neg 187 12.1 130 5.4 2 1 150/100 140/100 nil172 26 1 ckd 1 HCV 89 10.3 140 5.5 362 1 160/100 100/60 nil173 28 1 ckd 1 neg 172 19.7 130 4.4 8 1 130/90 140/90 nil174 68 1 ckd 1 neg 121 14.9 132 4.9 13 1 1 150/90 90/60 Hypotension175 37 1 ckd 1 neg 140 15.7 140 4.6 16 1 140/90 140/80 nil176 26 1 ckd 1 neg 160 17.2 140 4.6 23 1 150/90 150/80 nil
177 25 1 aki 1 neg 86 7.2 132 4.2 1 130/80 120/80
Paraquat
poisoning
nil
178 33 1 ckd 1 neg 166 16 142 4.8 23 1 150/90 140/80 Chest pain179 28 1 ckd 1 neg 172 16.6 142 4.8 62 1 150/90 130/90 nil180 23 1 ckd 1 neg 125 12.5 144 4.7 23 1 150/100 150/90 rigor181 17 1 ckd 1 neg 125 10 147 4.3 85 1 140/90 80/50 Hypotension182 29 1 ckd 1 neg 139 20.2 142 4.3 32 1 160/80 150/100 Cramps183 48 1 ckd 1 neg 230 26 120 6 5 1 160/100 150/100 nil184 53 1 ckd 1 neg 133 16.3 142 4.6 52 1 160/100 150/90 Cramps185 27 1 ckd 1 neg 107 15.7 137 4.6 56 1 160/100 150/80 nil186 38 1 ckd 1 neg 122 14.3 150 5.2 102 1 160/80 150/100 nil187 67 1 ckd 1 neg 158 9.6 149 6 46 1 1 150/80 130/90 rigor
188 28 1 aki 1 neg 96 10 146 5.6 2 1 120/90 130/80T2DM/HUN
rigor
189 34 1 Ckd 1 HCV 260 13.4 140 4.2 66 1 150/90 140/80 nil190 39 1 Ckd 1 HCV 189 14.3 142 3.8 49 1 140/90 130/80 nil
front page final 10.10.pdf (p.1-11)Dr Priya_thesis_08_10_18 .pdf (p.12-88)BIBLIOGRAPHY.pdf (p.89-92)Proforma.pdf (p.93-94)Concent form tamil.pdf (p.95)Master chart.pdf (p.96-101)